Evidence mapPaperPMID 41865719Full record

ArticleRedox biology2026

ACOD1-itaconate in macrophage attenuates oxidative stress and inflammation in benign airway stenosis by upregulating and transferring FTH1.

YiLin Chen, ChengFei Xu, Tao Luo, DongChen Shi, XinYi Guo, ChengCheng Yang, YuChao Dong, HaiDong Huang, YiFei Zhang, Zhe Zong and 6 more

Abstract read
In one paragraph

Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

YiLin ChenDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
ChengFei XuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China; Department of Critical Care Medicine, Jinling Hospital Affiliated Hospital of Nanjing University, Nanjing, China.
Tao LuoDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
DongChen ShiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
XinYi GuoDepartment of Information, No. 990 Hospital of the Chinese People's Liberation Army Joint Logistic Support Force, ZhuMaDian, China.
ChengCheng YangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
YuChao DongDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
HaiDong HuangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
YiFei ZhangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Zhe ZongDepartment of Critical Care Medicine, Jinling Hospital Affiliated Hospital of Nanjing University, Nanjing, China.
XiaoMin WangDepartment of Critical Care Medicine, Jinling Hospital Affiliated Hospital of Nanjing University, Nanjing, China.
ZhiRu XuNational Key Laboratory of Lead Druggability Research, China State Institute of Pharmaceutical Industry, Shanghai, China.
Yue ShiNational Key Laboratory of Lead Druggability Research, China State Institute of Pharmaceutical Industry, Shanghai, China.
ChaoFeng HanDepartment of Histology and Embryology, National Key Laboratory of Immunity and Inflammation, Naval Medical University, Shanghai, China. Electronic address: hcf@immunol.org.
Hui ShiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China. Electronic address: Shihui@smmu.edu.cn.
Chong BaiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China. Electronic address: Chongbai@smmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The oxidative stress of macrophage plays pivotal roles of acute and chronic inflammation and chronic fibrotic phases, in which the metabolic mechanism needs to be further explored. In our research, multi-omics analyses of human and murine during Benign airway stenosis (BAS) biopsy identified ACOD1 as a hallmark of immunometabolic regulation during acute inflammation stage. ACOD1 knockout aggravated both acute and chronic inflammation, which increased the granulation tissue formation. The ACOD1-itaconate axis, along with its derivative, 4-octyl itaconate (4-OI), orchestrated acute and chronic inflammation, which attenuated the fibrosis of BAS. 4-OI upregulated FTH1 expression in macrophages by activating NRF2, which effectively suppressed oxidative stress and acute inflammation. Furthermore, 4-OI promoted the packaging of FTH1 into macrophage-derived exosomes, which were transferred to fibroblasts in a SCARA5-dependent manner, inducing fibroblast ferroptosis and alleviating chronic fibrosis. In sum, this study illustrates that the ACOD1-itaconate metabolic axis decreases oxidative stress and inflammation in macrophage, which attenuates fibrosis by inducing FTH1 transfer, offering a therapeutic target for fibrotic airway diseases.

Indexed as

Airway ObstructionApoferritinsMacrophagesAnimalsCarboxy-LyasesConstriction, PathologicFemaleFerritinsFerroptosisHumansHydro-LyasesMaleMiceMice, Inbred C57BLOxidative StressOxidoreductasesACOD1 protein, humanAcod1 protein, mouseApoferritinsCarboxy-LyasesFerritinsFTH1 protein, humanFth1 protein, mouseHydro-Lyasesitaconic acidOxidoreductasesSCARA5 protein, mouseScavenger Receptors, Class ASuccinatesBenign airway stenosisFibrosisInflammationItaconateMacrophage

Identifiers

PMID41865719
PMCPMC13010451

What Socratic holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.